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Oligodendrocyte precursor cells facilitate neuronal lysosome release

ABSTRACT: Oligodendrocyte precursor cells facilitate neuronal lysosome release

PROVIDER: PRJNA1207448 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31912811_1.fastq.gz	Fastqsanger.gz
	SRR31912811_2.fastq.gz	Fastqsanger.gz
	SRR31912812_1.fastq.gz	Fastqsanger.gz
	SRR31912812_2.fastq.gz	Fastqsanger.gz
	SRR31912813_1.fastq.gz	Fastqsanger.gz

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Oligodendrocyte precursor cells facilitate neuronal lysosome release

Project description:Oligodendrocyte precursor cells (OPCs) shape brain function through complex mechanisms. We found that OPCs facilitate neuronal lysosome exocytosis by contacting neuronal somata. Reduced number or process branching of OPCs decreased these contacts, accompanied with lysosome accumulation and altered metabolism in neurons, and more senescent neurons with age. In Alzheimer's mouse models, OPC-neuron contacts were fewer, and lysosomes accumulated. Our findings are relevant for preventing aging-related pathologies and treatment of neurodegenerative diseases.

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Oligodendrocyte precursor cells facilitate neuronal lysosome release.

Project description:Oligodendrocyte precursor cells (OPCs) shape brain function through many non-canonical regulatory mechanisms beyond myelination. Here we show that OPCs form contacts with their processes on neuronal somata in a neuronal activity-dependent manner. These contacts facilitate exocytosis of neuronal lysosomes. A reduction in the number or branching of OPCs reduces these contacts, which is associated with lysosome accumulation and altered metabolism in neurons and more senescent neurons with age. A similar reduction in OPC branching and neuronal lysosome accumulation is seen in an early-stage mouse model of Alzheimer's disease. Our findings have implications for the prevention of age-related pathologies and the treatment of neurodegenerative diseases.

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GDE3 regulates oligodendrocyte precursor proliferation via release of soluble CNTFRα

Project description:GDE3 regulates oligodendrocyte precursor proliferation via release of soluble CNTFRα

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GDE3 regulates oligodendrocyte precursor proliferation via release of soluble CNTFRα

Project description:Oligodendrocyte development is tightly controlled by extrinsic signals; however, mechanisms that modulate cellular responses to these factors remain unclear. Six-transmembrane glycerophosphodiester phosphodiesterases (GDEs) are emerging as central regulators of cellular differentiation via their ability to shed glycosylphosphatidylinositol (GPI)-anchored proteins from the cell surface. We show here that GDE3 controls the pace of oligodendrocyte generation by negatively regulating oligodendrocyte precursor cell (OPC) proliferation. GDE3 inhibits OPC proliferation by stimulating ciliary neurotrophic factor (CNTF)-mediated signaling through release of CNTFRα, the ligand-binding component of the CNTF-receptor multiprotein complex, which can function as a soluble factor to activate CNTF signaling. GDE3 releases soluble CNTFRα by GPI-anchor cleavage from the plasma membrane and from extracellular vesicles (EVs) after co-recruitment of CNTFRα in EVs. These studies uncover new physiological roles for GDE3 in gliogenesis and identify GDE3 as a key regulator of CNTF-dependent regulation of OPC proliferation through release of CNTFRα.

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Investigation of Oligodendrocyte Precursor Cell Differentiation by Quantitative Proteomics

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